Pathways

PathWhiz ID Pathway Meta Data

PW122243

Pw122243 View Pathway
disease

Aspartylglucosaminuria

Homo sapiens
Aspartylglucosaminuria (AGU) is an inherited disease that is characterized by a decline in mental functioning, accompanied by an increase in skin, bone and joint issues. The disease is caused by a defect in an enzyme known as aspartylglucosaminidase (normally present in the liver and brain as well as other tissues). This enzyme plays a significant role in our bodies because it aids in breaking down certain sugars (for example, oligosaccharides) that are attached to specific proteins (for example, glycoproteins). Aspartylglucosaminuria itself is characterized as a lysosomal disease because it does deal with inadequate activity in an enzyme's function. Aspartylglucosaminidase functions to break down glycoproteins. These proteins are most abundant in the tissues of the body and in the surfaces of major organs, such as the liver, spleen, thyroid and nerves. When glycoproteins are not broken down, aspartylglucosaminidase backs up in the lysosomes along with other substances. This backup causes progressive damage to the tissues and organs. Aspartylglucosaminuria is a genetic condition that is inherited from both parents. The AGU patient is born with two copies of the mutated AGA gene. One copy comes from the mother’s egg and the other copy comes from the father’s sperm. In order to develop aspartylglucosaminuria, the individual must inherit changes in both of his AGU genes (autonomic recessive inheritance). When a person receives one changed form of the gene AGU from one of the parents, the individual is then classified as a carrier [Wikipedia].
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Creator: xuan cao

Created On: October 01, 2018 at 11:15

Last Updated: October 01, 2018 at 11:15

PW064753

Pw064753 View Pathway
physiological

chebulagic acid Metabolism

Homo sapiens
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Creator: Guest: Anonymous

Created On: June 10, 2018 at 16:58

Last Updated: June 10, 2018 at 16:58

PW122347

Pw122347 View Pathway
drug action

chebulagic acid Metabolism 1550463482

Homo sapiens
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Creator: Guest: Anonymous

Created On: February 17, 2019 at 21:19

Last Updated: February 17, 2019 at 21:19

PW122545

Pw122545 View Pathway
signaling

chebulagic acid Metabolism 1550463482 1563965617

Homo sapiens
BioPAX SVG SBGN SBML PWML All files (.zip)

Creator: Guest: Anonymous

Created On: July 24, 2019 at 04:54

Last Updated: July 24, 2019 at 04:54

PW013304

Pw013304 View Pathway
metabolic

Metabolic pathways

Mus musculus
bdnf symthesis
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Creator: Guest: Anonymous

Created On: May 02, 2017 at 07:48

Last Updated: May 02, 2017 at 07:48

PW002064

Pw002064 View Pathway
metabolic

1,6-Anhydro-N-acetylmuramic Acid Recycling

Escherichia coli
Most bacteria, including Escherichia coli, are composed of murein which protects and stabilizes the cell wall. Over half of the murein is broken down by Escherichia coli and recycled for the next generation. The main muropeptide is GlcNAc-anhydro-N-acetylmuramic acid (anhMurNAc)-l-Ala-γ-d-Glu-meso-Dap-d-Ala which enters the cytoplasm by AmpG protein. The peptide is then released from the muropeptide. 1,6-Anhydro-N-acetylmuramic acid (anhMurNAc) is recycled by its conversion to N-acetylglucosamine-phosphate (GlcNAc-P). The sugar is phosphorylated by anhydro-N-acetylmuramic acid kinase (AnmK) to produce MurNAc-P. Etherase cleaves MurNAc-P to produce N-acetyl-D-glucosamine 6-phosphate. The product can undergo further degradation or be recycled into peptidoglycan monomers. The pathway's final product is a peptidoglycan biosynthesis precursor, UDP-N-acetyl-α-D-muramate. The enzyme muropeptide ligase (mpl), attaches the recovered Ala-Glu-DAP tripeptide to the precursor UDP-N-acetyl-α-D-muramate to return to the peptide to the peptidoglycan biosynthetic pathway to synthesize the cell wall.
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Creator: Ana Marcu

Created On: October 09, 2015 at 12:00

Last Updated: October 09, 2015 at 12:00

PW123548

Pw123548 View Pathway
metabolic

1,6-Anhydro-N-acetylmuramic Acid Recycling

Pseudomonas aeruginosa
Most bacteria, including Escherichia coli, are composed of murein which protects and stabilizes the cell wall. Over half of the murein is broken down by Escherichia coli and recycled for the next generation. The main muropeptide is GlcNAc-anhydro-N-acetylmuramic acid (anhMurNAc)-l-Ala-γ-d-Glu-meso-Dap-d-Ala which enters the cytoplasm by AmpG protein. The peptide is then released from the muropeptide. 1,6-Anhydro-N-acetylmuramic acid (anhMurNAc) is recycled by its conversion to N-acetylglucosamine-phosphate (GlcNAc-P). The sugar is phosphorylated by anhydro-N-acetylmuramic acid kinase (AnmK) to produce MurNAc-P. Etherase cleaves MurNAc-P to produce N-acetyl-D-glucosamine 6-phosphate. The product can undergo further degradation or be recycled into peptidoglycan monomers. The pathway's final product is a peptidoglycan biosynthesis precursor, UDP-N-acetyl-α-D-muramate. The enzyme muropeptide ligase (mpl), attaches the recovered Ala-Glu-DAP tripeptide to the precursor UDP-N-acetyl-α-D-muramate to return to the peptide to the peptidoglycan biosynthetic pathway to synthesize the cell wall.
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Creator: Ana Marcu

Created On: August 12, 2019 at 22:30

Last Updated: August 12, 2019 at 22:30

PW064700

Pw064700 View Pathway
signaling

1.      Barrier

Homo sapiens
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Creator: Guest: Anonymous

Created On: March 16, 2018 at 21:18

Last Updated: March 16, 2018 at 21:18

PW000551

Pw000551 View Pathway
disease

11-beta-Hydroxylase Deficiency (CYP11B1)

Homo sapiens
11-beta-Hydroxylase Deficiency, also called congenital adrenal hyperplasia (CAH), is an autosomal recessive disorder and caused by a defective 11-beta-hydroxylase. 11-beta-hydroxylase catalyzes the conversion of cortexolone into cortisol which is useful for maintaining blood sugar levels and suppressing inflammation. This disorder is characterized by a large accumulation of cortexolone in the endoplasmic reticulum (ER). Symptoms of the disorder include abnormality of hair growth rate and menstrual cycle. It is estimated that 11-beta-hydroxylase deficiency affects 1 in 100,000 to 200,000 newborns.
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Creator: WishartLab

Created On: August 29, 2013 at 10:39

Last Updated: August 29, 2013 at 10:39

PW122119

Pw122119 View Pathway
disease

11-beta-Hydroxylase Deficiency (CYP11B1)

Rattus norvegicus
11-beta-Hydroxylase Deficiency, also called congenital adrenal hyperplasia (CAH), is an autosomal recessive disorder and caused by a defective 11-beta-hydroxylase. 11-beta-hydroxylase catalyzes the conversion of cortexolone into cortisol which is useful for maintaining blood sugar levels and suppressing inflammation. This disorder is characterized by a large accumulation of cortexolone in the endoplasmic reticulum (ER). Symptoms of the disorder include abnormality of hair growth rate and menstrual cycle. It is estimated that 11-beta-hydroxylase deficiency affects 1 in 100,000 to 200,000 newborns.
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Creator: Ana Marcu

Created On: September 10, 2018 at 15:52

Last Updated: September 10, 2018 at 15:52